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Associations between metabolic syndrome and urinary Na-to-K ratio and glomerular filtration rate in middle-aged adults regardless of Na and K intakes

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Abstract

Background

Intake of Na-to-K ratio (I-Na/K), urinary Na-to-K ratio (U-Na/K), and estimated glomerular filtration rate (GFR) have been reported to be risk factors of metabolic syndrome (MetS), but results are inconsistent. We examined the hypothesis that U-Na/K, GFR, and a preference for salty foods are associated with MetS risk and the hypothesis in 8540 adults aged over 40 years without chronic kidney disease.

Methods

Participants were categorized using a U-Na/K of < 2.1 (low-U-Na/k) and a GFR of < 60 mL/min (low-GFR). A GFR of 60–90 mL/min was considered as a normal level, since it is a normal or marginal disease state. Correlations and associations were determined using Pearson’s correlation coefficients and logistic regression analysis after adjusting for covariates related to MetS.

Results

U-Na/K, but not I-Na/K, was positively correlated with blood pressure (r2 = 0.20, P < 0.0001). The GFR was negatively correlated with age, gender, HOMA-B, and MetS (r2 = − 0.14 to − 0.595, P < 0.0001), and positively correlated with education, current smoking, and alcohol intake (r2 = 0.21 to 0.40, P < 0.0001). MetS risk had a positive association with the following combinations with low-U-Na/K + low-GFR, high-U-Na/K + high-GFR, and high-U-Na/K +low-GFR by 1.830-, 3.182-, and 3.696-fold, respectively, as compared with low-U-Na/K + high-GFR. Risks of the MetS components (abdominal obesity, hypertriglyceridemia, hypo-HDL-cholesterolemia, hypertension, and hyperglycemia) were similarly associated with U-Na/K and GFR, though hypertension had the strongest association. Hypertension risk had positive associations with low-U-Na/K + low-GFR, high-U-Na/K + high-GFR, and high-U-Na/K + low-GFR by 1.526-, 14.06-, and 7.079-fold, respectively, as compared with low-U-Na/K + high-GFR.

Conclusion

MetS risk was found to be associated with U-Na/K and GFR regardless of I-Na/K. Women need to maintain a high GFR to reduce the MetS risk, especially the risk of hypertension.

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Abbreviations

I-Na/K:

Intake of Na-to-K ratio

U-Na/K:

Urinary Na-to-K ratio

GFR:

Estimated glomerular filtration rate

MetS:

Metabolic syndrome

KoGES:

Korean Genome and Epidemiology Study

BP:

Blood pressure

SDs:

Standard deviations

HOMA:

Homeostasis model assessment

GFR:

Estimated GFR

SQFFQ:

Semi-quantitative food frequency questionnaire

ANOVA:

Analysis of variance

ORs:

Odds ratios

CIs:

95% confidence intervals

DBP:

Diastolic blood pressure

BMI:

Body mass index

References

  1. Kumari R, Kumar S, Kant R. An update on metabolic syndrome: metabolic risk markers and adipokines in the development of metabolic syndrome. Diabetes Metab Syndr. 2019;13(4):2409–17.

    Article  Google Scholar 

  2. Zhang J, Liu Q, Long S, Guo C, Tan H. Prevalence of metabolic syndrome and its risk factors among 10,348 police officers in a large city of China: a cross-sectional study. Medicine. 2019;98(40):e17306.

    Article  CAS  Google Scholar 

  3. Hoyas I, Leon-Sanz M. Nutritional challenges in metabolic syndrome. J Clin Med. 2019;8(9):1301.

    Article  CAS  Google Scholar 

  4. Vona R, Gambardella L, Cittadini C, Straface E, Pietraforte D. Biomarkers of oxidative stress in metabolic syndrome and associated diseases. Oxid Med Cell Longev. 2019;2019:8267234.

    Article  Google Scholar 

  5. Julibert A, et al. Total and subtypes of dietary fat intake and its association with components of the metabolic syndrome in a mediterranean population at high cardiovascular risk. Nutrients. 2019;11(7):E1493.

    Article  Google Scholar 

  6. Park S, Ahn J, Lee BK. Very-low-fat diets may be associated with increased risk of metabolic syndrome in the adult population. Clin Nutr. 2016;35(5):1159–67.

    Article  CAS  Google Scholar 

  7. Lee YJ, Song S, Song Y. High-carbohydrate diets and food patterns and their associations with metabolic disease in the korean population. Yonsei Med J. 2018;59(7):834–42.

    Article  CAS  Google Scholar 

  8. Li X, et al. Association of dietary sodium:potassium ratio with the metabolic syndrome in Chinese adults. Br J Nutr. 2018;120(6):612–8.

    Article  CAS  Google Scholar 

  9. Zhou J-Y, Song MY, Park S. Carbohydrate and sodium intake and physical activity interact with genetic risk scores of four genetic variants mainly related to lipid metabolism to modulate metabolic syndrome risk in Korean middle-aged adults. Br J Nutr. 2019;122(8):919–27.

    Article  CAS  Google Scholar 

  10. Murtaugh MA, et al. Relationship of sodium intake and blood pressure varies with energy intake: secondary analysis of the DASH (Dietary Approaches to Stop Hypertension)-sodium trial. Hypertension. 2018;71(5):858–65.

    Article  CAS  Google Scholar 

  11. Stone MS, Martyn L, Weaver CM. Potassium intake, bioavailability, hypertension, and glucose control. Nutrients. 2016;8(7):E444.

    Article  Google Scholar 

  12. Nomura N, Shoda W, Uchida S. Clinical importance of potassium intake and molecular mechanism of potassium regulation. Clin Exp Nephrol. 2019;23(10):1175–80.

    Article  Google Scholar 

  13. Murillo-de-Ozores AR, Gamba G, Castaneda-Bueno M. Molecular mechanisms for the regulation of blood pressure by potassium. Curr Top Membr. 2019;83:285–313.

    Article  CAS  Google Scholar 

  14. Do MH, Lee H-B, Oh M-J, Jhun H, Ha SK, Park H-Y. Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota. Eur J Nutr. 2020. https://doi.org/10.1007/s00394-020-02209-0.

    Article  PubMed  Google Scholar 

  15. Kogure M, et al. Multiple measurements of the urinary sodium-to-potassium ratio strongly related home hypertension: TMM Cohort Study. Hypertens Res. 2020;43(1):62–71.

    Article  CAS  Google Scholar 

  16. Jain N, Minhajuddin AT, Neeland IJ, Elsayed EF, Vega GL, Hedayati SS. Association of urinary sodium-to-potassium ratio with obesity in a multiethnic cohort. Am J Clin Nutr. 2014;99(5):992–8.

    Article  CAS  Google Scholar 

  17. Ge Z, et al. Association between 24 h urinary sodium and potassium excretion and the metabolic syndrome in Chinese adults: the Shandong and Ministry of Health Action on Salt and Hypertension (SMASH) study. Br J Nutr. 2015;113(6):996–1002.

    Article  CAS  Google Scholar 

  18. Musso N, Carloni B, Chiusano MC, Giusti M. Simple dietary advice reduces 24-hour urinary sodium excretion, blood pressure, and drug consumption in hypertensive patients. J Am Soc Hypertens. 2018;12(9):652–9.

    Article  CAS  Google Scholar 

  19. Stefansson VTN, Schei J, Solbu MD, Jenssen TG, Melsom T, Eriksen BO. Metabolic syndrome but not obesity measures are risk factors for accelerated age-related glomerular filtration rate decline in the general population. Kidney Int. 2018;93(5):1183–90.

    Article  CAS  Google Scholar 

  20. Ryu J, Lee C. Association of glycosylated hemoglobin with the gene encoding CDKAL1 in the Korean Association Resource (KARE) study. Hum Mutat. 2012;33(4):655–9.

    Article  CAS  Google Scholar 

  21. Daily JW, Park S. Interaction of BDNF rs6265 variants and energy and protein intake in the risk for glucose intolerance and type 2 diabetes in middle-aged adults. Nutrition. 2017;33:187–94.

    Article  CAS  Google Scholar 

  22. Park S, Daily JW, Zhang X, Jin HS, Lee HJ, Lee YH. Interactions with the MC4R rs17782313 variant, mental stress and energy intake and the risk of obesity in Genome Epidemiology Study. Nutr Metab. 2016;13:38.

    Article  Google Scholar 

  23. Park S, Zhang X, Lee NR, Jin HS. TRPV1 gene polymorphisms are associated with type 2 diabetes by their interaction with fat consumption in the Korean Genome Epidemiology Study. J Nutrigenet Nutrigenomics. 2016;9(1):47–61.

    Article  CAS  Google Scholar 

  24. Yoon C-Y, et al. High and low sodium intakes are associated with incident chronic kidney disease in patients with normal renal function and hypertension. Kidney Int. 2018;93(4):921–31.

    Article  CAS  Google Scholar 

  25. Abdulkader R, Burdmann EA, Lebrao ML, Duarte YAO, Zanetta DMT. Aging and decreased glomerular filtration rate: an elderly population-based study. PLoS One. 2017;12(12):e0189935.

    Article  Google Scholar 

  26. Eastwood SV, Tillin T, Chaturvedi N, Hughes AD. Ethnic differences in associations between blood pressure and stroke in South Asian and European men. Hypertension. 2015;66(3):481–8.

    Article  CAS  Google Scholar 

  27. Haddy FJ. Role of dietary salt in hypertension. Life Sci. 2006;79(17):1585–92.

    Article  CAS  Google Scholar 

  28. Ando K, Fujita T. Pathophysiology of salt sensitivity hypertension. Ann Med. 2012;44(Suppl 1):S119–26.

    Article  CAS  Google Scholar 

  29. Kawasaki T, Itoh K, Uezono K, Sasaki H. A simple method for estimating 24 h urinary sodium and potassium excretion from second morning voiding urine specimen in adults. Clin Exp Pharmacol Physiol. 1993;20(1):7–14.

    Article  CAS  Google Scholar 

  30. Naser AM, et al. Comparison of urinary sodium and blood pressure relationship from the spot versus 24-hour urine samples. J Am Heart Assoc. 2019;8(21):e013287.

    Article  Google Scholar 

  31. Wan ER, Cross J, Sofat R, Walsh SB. 24-hour vs. spot urinary sodium and potassium measurements in adult hypertensive patients: a cohort validation study. Am J Hypertens. 2019;32(10):983–91.

    Article  Google Scholar 

  32. Higo Y, et al. Association of the spot urine sodium-to-potassium ratio with blood pressure is independent of urinary Na and K levels: the Nagahama study. Hypertens Res. 2019;42(10):1624–30.

    Article  CAS  Google Scholar 

  33. Vaaraniemi K, et al. Lower glomerular filtration rate is associated with higher systemic vascular resistance in patients without prevalent kidney disease. J Clin Hypertens. 2014;16(10):722–8.

    Article  Google Scholar 

  34. Qiu Y, et al. Association of metabolic syndrome and its components with decreased estimated glomerular filtration rate in adults. Ann Nutr Metab. 2019;75(3):168–78.

    Article  CAS  Google Scholar 

  35. Eriksen BO, et al. Blood pressure and age-related GFR decline in the general population. BMC Nephrol. 2017;18(1):77.

    Article  Google Scholar 

  36. Rahman M, et al. The prevalence of reduced glomerular filtration rate in older hypertensive patients and its association with cardiovascular disease: a report from the antihypertensive and lipid-lowering treatment to prevent heart attack trial. Arch Intern Med. 2004;164(9):969–76.

    Article  Google Scholar 

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Funding

This research and the study design and methods were evaluated and approved for funding by the National Research Foundation (NRF-2019R1A2C1007203) in Korea.

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Contributions

SP: conceptualization, methodology, and original draft preparation. HJY and MYS: data analysis and writing–reviewing and editing. MJK: discussion.

Corresponding author

Correspondence to Sunmin Park.

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The authors declare that they have no conflict of interest.

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Yang, H.J., Song, M.Y., Kim, M.J. et al. Associations between metabolic syndrome and urinary Na-to-K ratio and glomerular filtration rate in middle-aged adults regardless of Na and K intakes. Clin Exp Nephrol 24, 1015–1024 (2020). https://doi.org/10.1007/s10157-020-01933-5

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